Source:http://linkedlifedata.com/resource/pubmed/id/10925260
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
|
pubmed:dateCreated |
2000-9-14
|
pubmed:abstractText |
Hapten sensitization through UV-exposed skin induces hapten-specific tolerance that can be adoptively transferred by injecting T lymphocytes into naive recipients. The exact phenotype of T cells responsible for inhibiting the immune response and their mode of action remain unclear. Evidence exists that CTLA-4 negatively regulates T cell activation. We addressed whether CTLA-4 is involved in the transfer of UV-induced tolerance. Injection of lymph node cells from mice that were sensitized with dinitrofluorobenzene (DNFB) through UV-irradiated skin inhibited induction of contact hypersensitivity against DNFB in the recipient animals. When CTLA-4+ cells were depleted, transfer of suppression was lost. Likewise, significantly fewer lymphocytes enriched for CTLA-4+ cells were necessary to transfer suppression than unfractionated cells. Expression of CTLA-4 appears to be functionally relevant, since in vivo injection of a blocking anti-CTLA-4 Ab was able to break UV-induced tolerance and inhibited transfer of suppression. Upon stimulation with dendritic cells in the presence of the water-soluble DNFB analogue, DNBS, CTLA-4+ T cells from DNFB-tolerized mice secreted high levels of IL-10, TGF-beta, and IFN-gamma; low levels of IL-2; and no IL-4, resembling the cytokine pattern of T regulatory 1 cells. Ab blocking of CTLA-4 resulted in inhibition of IL-10 release. Accordingly, transfer of tolerance was not observed when recipients were treated with an anti-IL-10 Ab. Hence we propose that T cells, possibly of the T regulatory 1 type, transfer UV-mediated suppression through the release of IL-10. Activation of CTLA-4 appears to be important in this process.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Blocking,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA-4 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Ctla4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoconjugates,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/abatacept
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0022-1767
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
165
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1824-31
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:10925260-Adoptive Transfer,
pubmed-meshheading:10925260-Animals,
pubmed-meshheading:10925260-Antibodies, Blocking,
pubmed-meshheading:10925260-Antigens, CD,
pubmed-meshheading:10925260-Antigens, Differentiation,
pubmed-meshheading:10925260-CTLA-4 Antigen,
pubmed-meshheading:10925260-Cells, Cultured,
pubmed-meshheading:10925260-Cytokines,
pubmed-meshheading:10925260-Immune Tolerance,
pubmed-meshheading:10925260-Immunoconjugates,
pubmed-meshheading:10925260-Immunosuppressive Agents,
pubmed-meshheading:10925260-Injections, Intraperitoneal,
pubmed-meshheading:10925260-Interleukin-10,
pubmed-meshheading:10925260-Lymphocyte Depletion,
pubmed-meshheading:10925260-Lymphocyte Transfusion,
pubmed-meshheading:10925260-Mice,
pubmed-meshheading:10925260-Mice, Inbred C3H,
pubmed-meshheading:10925260-T-Lymphocyte Subsets,
pubmed-meshheading:10925260-Ultraviolet Rays
|
pubmed:year |
2000
|
pubmed:articleTitle |
Evidence for functional relevance of CTLA-4 in ultraviolet-radiation-induced tolerance.
|
pubmed:affiliation |
Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, Department of Dermatology, University of Münster, Münster, Germany.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|